No abstract

Aim:The SFR (SpO 2 /FiO 2 ratio) offers a continuous, noninvasive reflection of pulmonary function regardless of whether the baby is ventilated or breathing spontaneously. We hypothesized that significant patent ductus arteriosus (PDA) shunting would impair pulmonary oxygen diffusion, reflected by decreased SFR; and that early PDA related decreases in SFR predict subsequent chronic lung disease (CLD).Methods: We retrospectively examined records from preterm neonates ≤30 weeks gestational age. Ductal shunting was graded for severity by first week echocardiogram. SFR was calculated as SpO 2 /FiO 2 and recorded on Day 7 of life and 36 weeks postmenstrual age (PMA).Results: We studied 104 infants: 65 with closed duct, 17 with hemodynamically insignificant PDA, and 22 with hemodynamically significant (hsPDAs). CLD developed in 9 (14%) of those with closed ducts; 6 (35%) of those with hisPDA; and in 12 (55%) of those with hsPDA (p = 0.005). SFR values at 1 week postnatally were decreased in those with hsPDA and with hisPDA as compared with those with closed ducts ; p = 0.00001). However, at 36 weeks only SFRs of babies with hsPDA remained significantly lower (467 [461−467] vs. 467 [413−471] vs. 369 [262−436] for closed vs. hisPDA vs. hsPDA respectively; p = 0.000148). Using ROC curve analysis, Week 1 SFR was strongly associated with hsPDA (area under curve [AUC] = 0.770; p < 0.0001) and highly predictive (AUC = 0.801; p < 0.0001) of CLD at 36 weeks PMA. Conclusion:Early decreases in SFR reflect both the acute and chronic pulmonary impact of PDA shunting, possibly providing the missing link supporting an association between hemodynamically significant PDA and subsequent CLD.

Perinatal thrombocytopenia has been shown to affect responsiveness to therapeutic ductal closure with cyclo-oxygenase inhibitors. This has not been studied in responsiveness to acetaminophen, which has less effect on platelet function. Objective: To evaluate whether thrombocytopenia affects ductal responsiveness to acetaminophen. Study Design: Retrospective review of preterm neonates <1500 gm. Echocardiograms were performed within the first week of life; if ductal status was found to be hemodynamically significant, infants were treated with acetaminophen. Results: We studied 254 infants. Fifty seven of these (22%) had a hemodynamically significant PDA (hsPDA) and were treated with acetaminophen. Forty (70%) of those treated responded with ductal closure after 1-2 courses of acetaminophen. Seventeen infants were considered non-responsive, requiring the addition of ibuprofen and/or surgical ligation. Sixty-seven of the 254 infants (26%) developed moderate thrombocytopenia [platelets <100,000] within the first ten days of life, more within the hsPDA group (54% vs. 18% p<0.001); however, no differences in platelet related parameters were observed when comparing infants with hsPDA who did or did not respond to acetaminophen treatment. Twenty-six of the 67 thrombocytopenic were already thrombocytopenic prior to acetaminophen treatment; and 19 of these 26 (73%) with pre-treatment thrombocytopenia responded to acetaminophen treatment – similar to the overall response rate of 70% . Conclusions: This study is the first to document that, in contrast to the cyclo-oxygenase inhibitors, there is no association between early neonatal thrombocytopenia and ductal therapeutic responsiveness to acetaminophen.

The SFR (Sp02/Fi02 ratio) offers a continuous, non-invasive reflection of pulmonary function regardless of whether the baby is ventilated or breathing spontaneously. We hypothesized that significant PDA shunting would impair pulmonary oxygen diffusion, in turn, reflected by decreased SFR; and that early PDA related decreases in SFR will predict subsequent chronic lung disease (CLD). Methods: We retrospectively examined records from preterm neonates <30 weeks gestational age. Ductal shunting was graded for severity by first week echocardiogram. SFR was calculated as SpO2/Fi02 and recorded on day 7 of life and at 36 weeks postmenstrual age (PMA). Results: We studied 104 infants: 65 with closed duct; 17 with hemodynamically insignificant PDA and 22 with hemodynamically significant (hsPDAs). CLD developed in 9 (14%) of those with closed ducts; 6 (35%) of those with hisPDA; and in 12 (55%) of those with hsPDA (p=0.005). Babies with hsPDA had significantly lower SFR values at both time points. SFRs in babies with hisPDA were decreased at 1 week postnatally, but were similar to those of babies with closed ducts at 36 weeks. SFR at 36 wks. was decreased only in infants with hsPDA [[467[461,467] vs. 467[413,471] vs. 369[262,436] respectively; p=0.000148]. Using ROC curve analysis, week 1 SFR was strongly associated with hsPDA (AUC=0.770; p<0.0001) and highly predictive (AUC=0.801; p<0.0001) of CLD at 36 weeks PMA. Conclusion: Early decreases in SFR reflect both the acute and chronic pulmonary impact of PDA shunting, possibly providing the missing link supporting an association between hemodynamically significant PDA and subsequent CLD.